This model is potentially applicable to the wide variety of cancers that co-mutate RB and PI3K/PTEN (for example breast, ovarian, glioma, prostate, and lung), and it will be interesting to determine the extent to which other cells similarly activate PI3K and Akt to inactivate FoxOs and suppress cell death during RB/E2F mediated expansion. This evidence concerns the gene AKT1 and glioma.